Sudden cardiac arrest (SCA) is based on the cessation of normal blood circulation due to failure of the heart to contract effectively, which most often leads to death (Sudden cardiac death (SCD) within less than one hour from the onset of symptoms. In the United States yearly about 600,000 people encounter a sudden cardiac arrest (SCA) with a mortality rate of about 460,000 people. SCA and SCD are frequently associated with cardiac arrhythmia, distinct from heart attacks, which are usually preceded by symptoms and signs.
Individuals that encounter sudden cardiac arrest (SCA) and/or sudden cardiac death (SCD) may be practically classified in three groups:
The first group includes individuals exhibiting cardiac disorders comprising mechanical pump failure. These patients show of myocardial ischemia with 80% of SCA; valvulopathy; hypertrophic cardiomyopathy (HCM); congenital anomalies; myocarditis; ruptured LV aneurysm; ruptured mitral papillary muscle; operative complications, Uhl's syndrome; acute intra-cardiac thrombosis; trauma, etc.; and electrical pump failure such as fibrosis of the His-Purkinje system; arrhythmogenic right ventricular dysplasia (ARVD) syndrome [Marcus]; prolonged Q-T interval syndromes; drugs; electrolytes abnormalities; hypothermia; Idiopathic ventricular fibrillation, etc.
The second group includes individuals exhibiting extra-cardiac disorders, comprising ailments of the central nervous system (CNS), the respiratory system, the vascular system, and the metabolic system. Examples for disorders of the CNS are cerebral edema; hemorrhage; tumor; meningitis; encephalitis; cerebral abscess; trauma; stroke; drugs; toxins; chemoreceptors—sympathetic and parasympathetic troubles, etc. Examples for respiratory disorders are pulmonary embolism; asthma; Eisenmenger syndrome; acute inflammatory and/or infection of the respiratory tract i.e. pharyngitis; laryngitis; tracheobronchitis; toxic inhalation i.e., carbon monoxide poisoning; drowning; Asphyxia; food aspiration; laryngospasm; etc. Examples for vascular disorders are massive hemorrhage due to trauma, dissecting or ruptured aortic aneurysm; hemoglobinopathy; mechanical obstruction venous return i.e. acute cardiac tamponade; etc. Examples for metabolic disorders are inflammatory syndromes, degenerative neuromuscular diseases; diabetic coma; electrolytes disturbances (e.g. hypo- or hyperkalemia, hypercalcemia (stoney heart); hypo- or hyperthyroidism; etc.
The third group includes individuals exhibiting miscellaneous disorders, such as Choking or Cafe coronary syndrome; postpartum amniotic fluid air embolism; alcohols; septicemia; sleep apnea; natural (i.e., advanced age >90 years); anaphylactic shock; homicides; electrocution; blunt head or chest traumatic shock (commotio cordis); Hypothermia/hyperthermia; extreme physical exercise (e.g. due to HCM in athletics <35 years and IHD in athetics >35 years); withdrawal syndrome; smokers, emotional factors (e.g. stress, depressions, etc.).
Presently known treatments of sudden cardiac arrest (SCA) usually involve cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC). These treatments imply a number of activities which may be subdivided in essentially five groups: cardiac massage, pharmacological supports, electrical (DC) shock, post-resuscitation Care and prophylaxis.
1.) Cardiac Massage:
a) Manual or standard CPR, usually performed by bystander with external compression of the chest wall at the midsternal level, and interrupted by ventilation assist in a compression/ventilation ratio of 30:2. High-Frequency (Rapid Compression Rate≈100 compressions per minute) may improve hemodynamics and 24-hour survival compared with standard CPR.
b) Mechanical CPR as an alternative technique to manual standard CPR with devices such as mechanical Piston CPR adapted to depress the sternum for optimizing chest compression and reducing rescuer fatigue. There exist a number of ways of performing mechanical CPR:
(i) Vest CPR, a circumferential thoracic vest that contains a pneumatic bladder to compress the chest in inflation/deflation rhythmic cycles assisted by an electromechanical generator. The device may be equipped with flat defibrillator electrodes, cutaneously positioned at the anterior chest wall and connected to an ECG control system.
(ii) AutoPulse, consisting of a board containing a motor, rechargeable batteries, and an 8-inch wide belt. The board is placed underneath a heart attack victim and the belt is strapped across the victim's chest. Once the device is turned on, the motor alternatively retracts the belt, producing chest compressions. The AutoPulse is lighter than the CPR vest (20 vs. 80 pounds), and able to produce up to 80 compressions per minute. The system could operate for 30-60 min on a single set of rechargeable batteries. FDA recognizes the system for application in USA.
(iii) Interposed abdominal compression (IAC-CPR) including manual compression of the abdomen by an extra rescuer during the chest compression. The interposed abdominal compression (IAC-CPR) uses a point located in the midline, halfway between the xiphoid process and the umbilicus. The abdominal compression should be strong enough to compress the abdominal aorta and vena cava (≈100 mmHg).
(iv) Phased Thoracic-Abdominal Compression-Decompression (PTACD-CPR, Lifestick) comprising a rigid frame attached to 2 adhesive pads. A smaller pad (20×17 cm) is placed on the mid-sternum, a larger pad (37×25 cm) on the epigastrium. The pads are fixed to the Lifestick prior to its placement on the patient. The Lifestick is used in a 15:2 compression-ventilation ratio, at 60 cycles per minute. The system is equipped with a metronome-driven 240° thoracic-abdominal phase shift (waltz-timing) as an indicator for optimal hemodynamic response. Also, it is equipped with a Tactile pressure indicator system to guide the abdominal compression force was limited to 18 to 28 kg (controlled by a colored LED display on the top of the frame). The display for the chest forces can be switched from a low (28 to 45 kg) setting to a medium (41 to 63 kg) or a high (54 to 82 kg) setting to achieve the target compression depth of 4 to 5 cm.
(v) CD-CPR (active compression-decompression-CPR) by decreasing the intrathoracic pressure during decompression phase of CPR is thought to enhance venous return and thereby “prime the pump” for the next compression. ACD-CPR is performed with a hand-held device equipped with a suction cup to actively lift the anterior chest during decompression.
(vi) Impedance Threshold Valve (ITV, or ResQ-Valve), which is associated with a lower intrathoracic pressure. When used with a compression/decompression device, the valve is inserted into a standard tracheal tube ventilation circuit and does not disrupt CPR performance. By preventing inspiration during chest decompression, the impedance threshold valve produces more negative intrathoracic pressure, enhancing blood return to the thorax.
(vii) Invasive CPR, in special situations of SCA, which require a direct cardiac massage through a thoracotomy or sternotomy incision.
(viii) Emergency cardiopulmonary bypass (CPB), which may be applied by a femoro-femoral technique without requiring a thoracotomy. Associations of hypothermia with CPB could improve neurologic outcome in certain occasion of SCA.
2.) Pharmacological Supports:
Direct intracardiac injections (ICI) of drugs (e.g., epinephrine, vasopressin and sodium bicarbonate), usually given by trained medical staff, through-into the right ventricle, and followed by continued external cardiac massage.
3.) DC Shock:
Using a standard external defibrillator device to deliver a transthoracic electrical shock for restoring normal cardiac rhythm which usually involves the use of hand-held paddle electrodes or self-adhesive patch electrodes. Paddles are usually placed in an anterolateral position between the ventricular apex and the right infraclavicular area. In the anteroposterior position, paddles are placed over the sternum and the interscapular space. Additional devices may be such as: a) Automated external defibrillators (AEDs) being portable special defibrillators that untrained bystanders may use. The AEDs are programmed to give an electric shock if they detect any dangerous arrhythmia and prevent giving an unnecessary shock to someone who may have fainted. b) Implantable cardioverter defibrillator (ICD) which is a pacemaker like device having wires with electrodes on the ends that connect to the heart's chambers (right atrium and right ventricle). If the ICD detects a dangerous heart rhythm, it will give an electric shock to restore the heart's normal rhythm. Patients might need medicinal support to avoid irregular heartbeats that can trigger the ICD.
4.) Post-Resuscitation Care:
After initial CPR, victims require support to restore cardiac and organ functions. These include a hemodynamic support, prevention of hyper or hypothermia, control of blood sugar and avoiding a routine hyperventilation. As more than half of post-resuscitation syndrome deaths occur within 24 hours after the ROSC, due to dysfunction of the microcirculation, this leads to metabolic disorders eventually resulting in multiple organs failure.
5.) Prophylaxis:
Procedures such as the microvolt T-wave alternans (TWA), and programmed ventricular stimulation (PVS) may represent a promising approach to predict fatal arrhythmias in high-risk ischemic heart diseases patients.
Even though a number of devices and means adjunctive to standard manual CPR have been shown to improve the efficacy of CPR in SCA patients, the survival rate still remains quite poor. These drawbacks are deemed to be caused at least in part by non appropriately selected resuscitation methods and therapeutic concepts.
In selecting a particular concept attention is to be given to cardiovascular physio-pathology, the cardiothoracic anatomy, and the hemodynamics/hemorheology.
The contraction of the cardiac muscle is initiated by electrical impulses, which are the result of polarization/depolarization mechanisms of particular cardiac cells (termed pacemaker cells). These pacemaker cells represent only one percent (1%) of cardiac cells and create rhythmical impulses that are transferred from said through a conducting system and adjacent cells.
Anatomically, the electrical impulses creating system of the heart is composed of three entities: a) the sinoatrial node (SA node—the primary pacemaker zone), which is positioned on the wall of the right atrium (near the entrance of the superior vena cava); b) the atrioventricular Node (AV node—the secondary pacemaker zone), localized near the apex of the triangle of Koch inside the right atrium; and c) the bundle of His and Purkinje fibers, which are the continuity of the electrical conducting system of the heart.
The pacemaker cells spontaneously depolarize, giving a native rate of about 100 bpm, which rate is controlled and modified by the sympathetic and parasympathetic autonomic nervous system, resulting in heart rate in an adult individual of around 70 bpm. If the SA node does not function the AV node (secondary pacemaker) will step in producing a spontaneous heart rate of around 40-60 bpm. If both, the primary and secondary pacemakers fail to produce electrical signals the HIS and the Purkinje fibers will produce a spontaneous action potential at a rate of about 30-40 beats per minute.
The heart beat as such is normally controlled only by the SA node in that its action potentials are released more often. The action potential generated by the SA node passes down the cardiac conduction system, and arrives before the other cells had a chance to generate their own spontaneous action potential.
For the generation of an action potential a pacemaker cell moves through 5 phases (numbered 0-4): Phase 4 is characterized by the resting membrane potential (−60 mV to −70 mV), which is caused by a continuous outflow potassium ions through ion channel proteins in the cells membrane. During Phase 0 a rapid depolarization occurs, which is mainly caused by an influx of Na+ and Ca2+ ions. During Phase 1 the Na+ channels are inactivated due to the movement of K+ (efflux) and Cl− ions. Phase 2 represents a “plateau” phase of the cardiac action potential due to a balanced influx of Ca2+ and efflux of K+ ions. During Phase 3 a “repolarization” of the action potential occurs, with closure of the Ca2+ channels, and slowing of K+ efflux.
As is appreciated a heartbeat depends on a reaction on/within the membranes of pacemakers cells.
This reaction may be induced by a sudden filling of the empty right atrium, effecting direct snapping impacts at the membranes of the pacemaker cells, and also indirectly by wall stretching. In other words, a heartbeat primarily depends on an endothelial elastic membrane function mediated by shear stress which stress is induced by blood flow dynamics at the right heart cavities. The first heartbeat in a human appears around the 21st gestational day, induced by the direct effect of the placental circulation endothelial shear stress (ESS) and maternal neurohumoral factors upon the right atrium pacemaker cells. Afterwards heartbeat will continue and be maintained by blood flow that stimulates the pacemaker cells mechanically via the pulsatile impacts of shear stress, and/or chemically with combinations of neurohumoral factors and electrolytes channels.
In case of a cardiac arrest the main target for reviving blood circulation is to stimulate the pacemaker cells inside the right atrium first, which is, however, difficult to achieve with current CPR methods. As is known (and shown in FIG. 1), the sternum is separated from the heart by several centimeters. As a result chest compressions must be strong enough to compress the hard thoracic cage (1, 2), and then also the mobile soft mediastinal and cardiac structures up to the thoracic aorta (6), which is located almost far backward on the dorsal vertebrae (7). However, any revival of cerebral and coronary circulation flow depends on systemic arterial blood flow ejected by the left ventricle (4), following a left atrium (8) preload. Anatomically, the left cardiac cavities are positioned posterior to the right heart chambers, which means that the systole of the compressed right ventricle will be delivered first into the pulmonary circulation to follow the normal cardiac cycle. The pulmonary circulation collapsed due to cardiac arrest refutes this unrealistic imagination of systemic preload-afterload dependency of cardiac massage.
Hence, due to the anatomical position of the heart currently used cardiac massages have few chances of triggering a heartbeat. In addition, these current procedures repeat successive chest blows—regardless of the physiological action potential of the cardiac phases—which may even lead to a commotio cordis or a re-arrest of the heart.
A human adult contains roughly 4-6 l blood, with the venous system holding almost about 70-80% of the blood volume. An adult heart harbors around 400-500 ml, and the systemic arteries about 3-5% of the blood volume.
Under operation conditions the heart and the blood circulation system create a (blood) pressure, which is endogeneously higher in the arteries than in the venous system. Within about 30 seconds following a sudden cardiac arrest the cardiovascular pressure is equalized in the blood circulatory system since the arterial pressure falls and the venous pressure rises as some of the arterial blood moves into the veins during pressure equalization.
During CPR an elevated coronary perfusion pressure (CPP) of at least 15 mm Hg is required for return of spontaneous circulation (ROSC). It seems almost impossible to restore metabolic processes and organ perfusions properly by compressing such few amounts of stagnant intra-ventricular blood volume (about 400 ml), unequally divided between left and right cardiac chambers. Consequently blood flow during CPR is usually inadequate to ensure vital organs perfusions.
Drawbacks of the devices currently applied, such as manual or piston CPR, include a limitation of recoil of the thorax as well as venous return during decompression. Interferences with defibrillation efforts may occur which may cause re-ventricular fibrillation (e.g. commotio cordis). Rib fractures occur frequently, as well as cardiac injury and pericardial tamponade due to extra force and energy applied to the chest wall during ACD-CPR. Devices such as the IAC-CPR are contraindicated in patients with aortic aneurysms, pregnancy, or recent abdominal surgery. Almost all mechanical devices are limited to in-hospital resuscitations requesting trained staff with considerable costs. The efficacy and safety of mechanical devices have not been demonstrated for infants and children, their use is still limited to adults. The FDA does not approve most of the current CPR mechanical devices. Invasive CPR is still limited to in-hospital patients with specific indications including i) cardiac arrest caused by hypothermia, pulmonary embolism, or pericardial tamponade; ii) chest deformity where closed-chest CPR is ineffective; and iii) penetrating abdominal trauma with deterioration and cardiac arrest. The use of open-chest direct cardiac massage can be considered under special circumstances but should not be performed simply as a late last-ditch effort.
There are also drawbacks associated with pharmacological supports. As is acknowledged intra and extracellular electrolytes play a crucial role in the heartbeat mechanism and are usually disturbed by SCA. Current IV pharmacological CPR supports are ineffective due to a stagnant circulation. Drug treatment by direct ICI technique is also less effective and associated with quite annoying side effects. Furthermore, a prospective randomized controlled trial confirmed that routine use of high-dose epinephrine was not beneficial and may actually increase rates of morbidity and mortality.
The benefits of DC shock are still debated, as controversies between chest compression first versus DC shock first remain unresolved. This is mainly due to the fact that most SCA victims demonstrate a non-perfusion phase (prolonged depolarization) for several minutes, which necessitates immediate massage. A successful DC shock must be strong enough to affect pacemaker cells that represent only about 1% of cardiac myocytes. A prolonged depolarization after strong shocks may cause myocardial necrosis caused by an electroporation, i.e. a rupture of cardiac cell membrane. An associated tachyarrhythmia is one of the most common complications associated with DC shocks, which is contra-indicated in case of digitalis toxicity. Thromboembolic accidents are more likely to occur in patients with atrial fibrillation (AF) who have been treated with DC shocks without proper anticoagulation. Painful skin burns have been reported for 20-25% of patients after DC shocks due to technical reasons. This is usually attributed to the paddles size, skin-to-electrode contact and waveforms types (i.e. monophasic or biphasic). Some studies have confirmed that the anteroposterior position DC shock is superior because it requires less energy to reverse AF. In a matter of fact, only 4% to 5% of the shocking energy actually reaches the heart due to deviation of this electric field. Also, pulmonary edema has been reported after DC shocks.
In the prior art a number of medical devices for assisting during/after a cardiac arrest which do not focus on chest compressions are known.
WO 2008/000111 discloses a neonate or infant pulsating wear to obtain the puls. The wear exhibits a multilayer structure comprising an elastic inner layer contacted with the body of the infant, an outer layer isolating the body of the infant, and a middle layer between the inner layer and the outer layer. Said middle layer contains a pulsant cyclic liquid and the outer layer is harder than the inner layer.
WO 2010/070018 pertains to a pulsatile and non-invasive device for circulatory assistance, which device promotes the circulation of a volume of blood in the body of a subject. The device comprises a flexible multi-layer structure designed to be applied to at least a part of the subject's body and exhibits a flexible inner layer towards the body of said subject and a more rigid outer layer. Pulsation means are connected to said multi-layer structure in such a way that the assembly composed of the structure and of the pulsation means is leaktight. Utilizing the pulsation means pulsations are created between said inner and outer layers by way of a pulsation fluid. Each of the pulsations propagate progressively in the direction of venous return along that part of the body of said subject when said structure is arranged to this particular part of the body.
US 2012/0232331 discloses a circulatory assist device (CAD) that is minimally invasive and which improves the hemodynamics, i.e. the overall microcirculation in organs, and the restoration and preservation of deficient endothelial function in a patient. The device must be placed externally to the patient's body and connected by at least a pipe and/or a specific connection element to increase the preload of the right ventricle so as to improve oxygenation of the myocardium and so as to improve its contractility, and/or unload the left ventricle and diffuse regular pulsatile flow in the proximity of the aortic root so as to improve the hemodynamics of the left ventricle of the heart, and/or stimulate the endothelium mechanically by shear stress enhancement so as to release several mediators of endothelial vasodilators like nitric oxide, to reduce the systemic and pulmonary afterload.
WO 2009/153491 relates to a device for applying a predetermined pulsatile pressure to a medical device. The disclosed device comprises a withdrawing means designed to withdraw fluid from a source of fluid in continuous flow at high pressure, a conversion means designed to convert said fluid into a fluid in a pulsatile flow at low pressure, at least one application means for applying said fluid as a low-pressure pulsatile flow to said medical device, and a means for removing said fluid.
Yet, there still exists a need in the art for a device that improves the outcome of a CPR treatment.